Geddes C C, Jardine A G
Renal Unit, Western Infirmary, Glasgow, United Kingdom.
Minerva Urol Nefrol. 2002 Mar;54(1):29-36.
Atherosclerotic renal artery stenosis (ARAS) is an increasingly common cause of secondary hypertension and progressive chronic renal failure. Recent studies provide valuable information about the pathophysiology, natural history, diagnosis and treatment of ARAS. The pathophysiology of ARAS is more complex than experimental models using clipped renal arteries because the renal artery narrowing is gradual, may be bilateral, may affect smaller intra-renal arteries and other co-existing nephropathies are often present. Patients with ARAS have high mortality due to associated co-morbidity and progression of renal failure may be less common than previously thought. Magnetic resonance arteriography offers great promise for diagnosing of ARAS as it is non-invasive and can provide data on kidney function. In patients with ARAS, the co-existence of atherosclerotic disease in other vascular beds means that aspirin, blood pressure reduction, advice to stop smoking and lipid lowering therapy are likely to be associated with reduced vascular events. The effect of these approaches on the progression of ARAS is unclear but likely to be beneficial. Re-vascularisation of occluded renal arteries is an attractive option for treatment of ARAS but data from the few randomised controlled studies that have been published do not support its widespread application. Arterial stenting has a higher technical success rate than angioplasty while surgical revascularisation does not appear to improve outcome compared with angioplasty. Recent studies examining functional and histological features of kidneys supplied by atherosclerotic stenosed renal arteries may explain why revascularisation is not always beneficial. The results of on-going studies may identify sub-groups of patients with ARAS who gain a clear benefit from re-vascularisation. In the meantime it seems reasonable to attempt re-vascularisation in the following circumstances: severe hypertension resistant to medical therapy, rapidly progressive renal failure with no obvious cause other than ARAS and recurrent flash pulmonary oedema.
动脉粥样硬化性肾动脉狭窄（ARAS）是继发性高血压和进行性慢性肾衰竭日益常见的病因。近期研究提供了关于ARAS的病理生理学、自然病程、诊断和治疗的有价值信息。ARAS的病理生理学比使用肾动脉夹闭的实验模型更为复杂，因为肾动脉狭窄是渐进性的，可能是双侧的，可能影响较小的肾内动脉，并且常常存在其他并存的肾病。由于相关的合并症，ARAS患者死亡率较高，肾衰竭的进展可能比以前认为的要少见。磁共振血管造影术在诊断ARAS方面前景广阔，因为它是非侵入性的，并且可以提供肾功能数据。在ARAS患者中，其他血管床存在动脉粥样硬化疾病意味着阿司匹林、降低血压、戒烟建议和降脂治疗可能与血管事件减少相关。这些方法对ARAS进展的影响尚不清楚，但可能有益。闭塞性肾动脉的血管重建是治疗ARAS的一个有吸引力的选择，但已发表的少数随机对照研究的数据不支持其广泛应用。动脉支架置入术的技术成功率高于血管成形术，而与血管成形术相比，外科血管重建术似乎并未改善预后。近期对动脉粥样硬化性狭窄肾动脉供血的肾脏的功能和组织学特征进行研究，可能解释了为什么血管重建并不总是有益的。正在进行的研究结果可能会确定从血管重建中明显获益的ARAS患者亚组。与此同时，在以下情况下尝试血管重建似乎是合理的：对药物治疗耐药的重度高血压、除ARAS外无明显病因的快速进行性肾衰竭以及反复发生的急性肺水肿。
